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| ORIGINAL ARTICLE |
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| Year : 2021 | Volume
: 5
| Issue : 4 | Page : 440-445 |
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Histopathological changes in placenta in pregnancy-induced hypertensive patients and correlation with fetal outcome – a tertiary care hospital study
Aparajita Samaddar, Utso Guha Roy, Ipsita Saha, Srishtidhar Mangal
Department of Pathology, Medical College and Hospital, Kolkata, West Bengal, India
| Date of Submission | 17-Jul-2021 |
| Date of Acceptance | 15-Oct-2021 |
| Date of Web Publication | 14-Dec-2021 |
Correspondence Address:
Srishtidhar Mangal
Department of Pathology, Medical College and Hospital, 88 College Street, Kolkata - 700 073, West Bengal
India
 Source of Support: None, Conflict of Interest: None
DOI: 10.4103/bbrj.bbrj_147_21
Background: The placenta, fetus, and mother form a composite functional equilibrium during prenatal period. The dysfunction of placenta often leads to preeclampsia/eclampsia. They remain the major causes of maternal and perinatal mortality. It has been revealed that there is a clear relationship between placental pathology and intrauterine growth restriction in preeclampsia. Aim of this study was to evaluate the histomorphological changes of placenta in pregnancy induced hypertensive disorders and to compare those with normal placenta and to correlate the findings with foetal outcome in terms of APGAR score and birth weights of newborn babies. Materials and Methods: This was an analytical cross-sectional study. We included 50 pregnant women with pregnancy induced hypertension as cases and 50 normotensive pregnant women as controls. Specimens of placenta from each cases and controls were collected after delivery and processed by routine histopathology technique. We looked for morphological and histological changes in placenta. We also collected the data on APGAR scores, birth weight and fetal death, if any. Microsoft Excel 2013 and Minitab version 17 were utilized for statistical analysis. Results: We found statistically significant reduction in placental weight, diameter and thickness among cases compared to controls and there is also a strong correlation with the histopathological changes of placenta in hypertensive mothers to fetal weight. Birth weights of newborns to hypertensive mothers were significantly lower than those of normotensive mothers. Conclusion: Hypertensive disorders of Pregnancy causes significant histomorphological changes in placenta leading to adverse foetal outcome.
Keywords: Fetal outcome, histomorphological changes, pregnancy-induced hypertension
How to cite this article:
Samaddar A, Roy UG, Saha I, Mangal S. Histopathological changes in placenta in pregnancy-induced hypertensive patients and correlation with fetal outcome – a tertiary care hospital study. Biomed Biotechnol Res J 2021;5:440-5 |
How to cite this URL:
Samaddar A, Roy UG, Saha I, Mangal S. Histopathological changes in placenta in pregnancy-induced hypertensive patients and correlation with fetal outcome – a tertiary care hospital study. Biomed Biotechnol Res J [serial online] 2021 [cited 2023 Jun 9];5:440-5. Available from: https://www.bmbtrj.org/text.asp?2021/5/4/440/332505 |
| Introduction | |  |
The triad of placenta, fetus, and mother continues to form a composite functional equilibrium during prenatal period, and dysfunction of any one of them can jeopardize the others. The dysfunction of the placenta often could lead to preeclampsia (PE)/eclampsia. PE is a pregnancy-associated pathology that is characterized by poor placentation and endothelial dysfunction.[1] PE is clinically defined by new-onset hypertension (systolic and diastolic blood pressures of 140 and 90 mmHg, respectively), proteinuria (300 mg over 24 h), and organ dysfunction after 20 weeks of gestation.[2] It carries a significant risk of progression to eclampsia, in which PE patients develop convulsions, resulting in multiple complications and maternal and fetal death.[3] PE and eclampsia remain the major causes of maternal and perinatal mortality and morbidity worldwide, causing 12%–15% of direct maternal deaths.[4] The histological changes in preeclamptic/eclamptic placentas include infarcts, increased syncytial knots, subchorionic fibrin deposition, calcification, hypovascularity of the villi, cytotrophoblastic proliferation, thickening of the trophoblastic membrane, obliterative enlarged endothelial cells in the fetal capillaries, and atherosis of the spiral arteries in the placental bed.[5] In recent years, it has been revealed that there is a clear relationship between placental pathology and intrauterine growth restriction in PE.[6] However, most of the studies so far on placental changes in PE and eclampsia were done on Caucasians and African blacks living in Western countries. Therefore, there is a need for an indigenous study to evaluate the placentas of these patients and develop indigenous database for patients' management. The aim of this study was to evaluate the morphological changes of placenta in pregnancy-induced hypertensive disorders with respect to placental weight, diameter, and thickness of placenta along with histopathological changes and to compare those with placenta of normotensive mothers. We also tried to correlate the histomorphological findings to the neonatal outcome in terms of Apgar score at 1 min and 5 min and birth weights of the newborn babies.
| Methods | | |
The present study was conducted after obtaining Institutional Ethical Clearance (No. MC/Kol/IEC/Non-spon/334/08-2016 dated 24th Sept, 2016) and informed consents from all the participants. This study was done in the departments of pathology and gynecology and obstetrics in a tertiary care hospital of West Bengal over a period of 2 years. This was an analytical cross-sectional study. We included fifty pregnant women with pregnancy-induced hypertension (PIH) or PE or eclampsia or chronic hypertension or superimposed PE as cases and fifty normal pregnant women as controls. The diagnosis of the different types of hypertensive disorders in pregnancy was done considering the definitions provided by the National High Blood Pressure Education Program, 2000. PIH is defined as blood pressure elevation (>140/90 mm Hg) detected for the first time after 20 weeks of gestation without proteinuria. Pre- eclampsia is defined as a condition where PIH is associated with new onset proteinuria (≥300 mg urinary protein excretion per 24 hours). Again when pre-eclampsia is complicated by seizures that cannot be attributed to any other cause is defined as eclampsia. Superimposed PE is a condition where a woman with chronic hypertension develops new-onset proteinuria after 20 weeks of gestation. Chronic hypertension is defined as hypertension (>140/90 mm Hg) that is present and observable before pregnancy or that is diagnosed before the 20th week of gestation. Hypertension that is diagnosed for the first time during pregnancy and that does not resolve postpartum is also classified as chronic hypertension. Pregnant women having complications such as severe anemia, placenta previa, abruption placentae, multiple pregnancies, gestational diabetes, and severe respiratory or cardiovascular diseases were excluded from this study. Control group included normotensive pregnant women with other criteria as similar to cases. Prior to sample collection, written consent was taken from both cases and controls for ethical purposes. We collected the specimen of placenta from each case and control after delivery. After collection of the sample of placenta, it was placed in 10% Formalin solution in a large container for fixation. Large container was preferred to avoid the distortion of the shape of placenta. The volume of the fixative was at least 10 times the volume of the specimen to allow adequate fixation of the tissue. We also collected the data on neonatal outcome including Apgar scores at 1 min and at 5 min after birth, birth weight, any gross congenital anomaly, or fetal death, if any.
After adequate fixation in formalin, gross examination of the collected placentas was done to note the weight, thickness, diameter, infarctions, calcifications, any abnormalities of the umbilicus, or its insertion. Sections were taken from relevant areas of both fetal and maternal surfaces of placenta and also from umbilical cord for the study. Five-micrometer thickness sections were cut by microtome and were stained by routine hematoxylin and eosin stain for microscopical evaluation. We looked for subchorionic fibrin, retroplacental hematoma, infarction, and calcification in each section.
All the data collected were analyzed in terms of their mathematical mean value. Pearson correlation between variables was done to establish statistical correlation between placental diameter and birth weight, placental thickness, and birth weight. Relative risk and odds ratio were calculated to estimate the risk of subchorionic fibrin, retroplacental hematoma, infarction, calcification, and neonatal death due to PIH and to estimate the strength of association between PIH and the aforesaid outcomes, respectively. Two-sample t-test was performed and test of significance was done in terms of 95% confidence interval to assess the distinctive difference in data between cases and controls. For mathematical and statistical calculation purpose, Microsoft Excel 2013(Comdex, Las Vegus, USA) and Minitab version 17 (Statecollege, Pennsylvania State, USA) were utilized.
This study was approved by the Ethics Committee of Medical College, Kolkata.
| Results | | |
The rate of incidence of gestational hypertension, PE, eclampsia, superimposed PE, and chronic hypertension among cases was found to be 38%, 36%, 8%, 10%, and 8%, respectively, in this study [Diagram 1]. The distribution of cases and controls according to age was noted. Most of the participants were in the age group of 22–25 years. We found that the percentage of cases of PE, eclampsia, and superimposed PE was much higher in the extremes of age groups, i.e. below 21 years and more than 30 years, with the rates of 63% and 71%, respectively. Hence, we concluded that age has an important influence on the incidence of hypertensive disorders of pregnancy [Diagram 2]. Influence of maternal gravid status on the occurrence of PIH was assessed and it was found that the occurrence of PIH was more among multigravida than in primigravida (51.8% vs. 47.7%. We observed that the incidence of preterm delivery was 32% among cases whereas it was found to be only 8% among cases. We compared the placental weight among the cases and controls. The mean placental weight among cases and controls was found to be 440.8 g and 540 g, respectively (P < 0.05), which is statistically significant [Table 1]. Again, we noted a statistically significant (P < 0.05) reduction in placental diameter and thickness among cases compared to controls. The mean placental diameter and thickness among cases and controls were found to be 14.44 cm and 17.58 cm, respectively, and 1.610 cm and 2.040 cm, respectively [Table 1]. Regarding histopathological findings, 50% of placentas studied in cases showed the presence of subchorionic fibrin, whereas only 10% of placentas from the control group showed the same [Figure 1]. Moreover, PIH contributed the maximum number of cases, constituting 40% of total occurrence of subchorionic fibrin. Superimposed preeclampsia held the lowest of value with 4% occurrence among the cases. Placentas from 24% of cases showed the presence retroplacental hematoma, whereas only 6% of placentas from the control group showed similar findings [Figure 2]. In this study, we found placental infarction among 46% of cases, whereas only 10% of controls showed the same. Again, PE contributed the maximum number of cases, constituting 47% of total occurrence of infarction, and chronic hypertension held the lowest of value with 4.3% occurrence among the cases [Figure 3]. Similarly, calcification was also found to be more common among cases comprising 44% of cases compared to only 6% among controls [Table 2]. Among which, PIH contributed the maximum number of cases, constituting 45% of total occurrence of calcification, and eclampsia held the lowest of value with 4.5% occurrence among the cases [Figure 4]. | Table 2: Histopathological findings in placenta among cases and controls
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Relative risk and odds ratio were calculated to estimate the risk of subchorionic fibrin, retroplacental hematoma, infarction, and calcification due to PIH and to estimate the strength of association between PIH and the aforesaid outcomes, respectively [Table 3]. All of the above histological findings showed a significant correlation with PIH (P < 0.05). | Table 3: Association of histopathological finding with low birth weight of the baby
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In this study, we also found that there is a statistically significant reduction in birth weight (P < 0.05) among newborns to hypertensive mothers. The mean birth weight of newborns to hypertensive and normotensive mothers was found to be 2464 g and 2847 g, respectively. It was observed that the incidence of babies with low Apgar score was more among hypertensive mothers than in the control group, the rates being 38% and 4%, respectively. Total three cases (6%) of neonatal mortality were noted among the hypertensive study group, whereas one case (2%) of neonatal death occurred in the control group. Although there is a marked difference in incidence, the data were not significant which was evident from P = 0.33.
Association of histopathological finding such as subchorionic fibrin with low birth weight of the baby was calculated using odds ratio and relative risk, and the data were found to be statistically significant [Table 3]
In the present study, we found that the mean fetoplacental ratio was higher in the hypertensive group than in the control group, but the data were not statistically significant.
| Discussion | | |
The placental pathology plays an important role in perinatal mortality in patients with PIH. Hence, the understanding of placental pathology is of utmost importance. In this study, we observed the morphological and histological changes of placenta in patients with PIH, preeclampsia, and eclampsia. We also compared the changes with that of normal pregnancy. We tried to find out the correlation between the histopathological changes and the fetal outcome. In this study, we observed that the mean (±standard deviation [SD]) placental diameter in the hypertensive group was 14.44 ± 2.18 cm whereas that in the control group was 17.58 ± 1.63 cm and the difference was statistically significant (P < 0.05). Teasdale, 1987, found a significant reduction of transverse diameter in the PE group; this reduction seems to be due to the small size of placenta in the PE group.[7] Cibils reported that the placentae from hypertensive patients were significantly smaller than the normal, suggesting that the pathologic process interferes with the normal placental growth.[8] Similar findings have been reported by Londhe and Mane and Salmani et al. They found a significant reduction in transverse diameter of preeclamptic placentae.[9],[10]
The mean (±SD) placental thickness was 1.610 ± 0.583 cm among the cases whereas it was 2.040 ± 0.513 cm among the controls. The P value was <0.05, so the data are statistically significant. Sapna Shecade et al. in 2015 in their study showed that the mean placental thickness in the control group was found to be 2.3 ± 0.43 cm and that in cases was found to be 1.8 ± 0.49 cm which substantiates the findings from our study.[11]
In the current study, placental weight of the entire study population was recorded. It was observed that the mean placental weight in the hypertensive group was 440.8 g, and in the control population, it was 540 g. Salmani et al. also investigated the correlation between PIH and placental abnormalities in 2014. They concluded that the weight of placenta was less in the study group when compared with the control group.[10] Their observation was correlated well with the previous studies done by various workers. Bazaz et al. reported five cases of toxemia of pregnancy with placental weight <300 g.[12] Nobis and Das, in their study (1991), observed that the placental weight in toxemic cases varies from 279 to 407 g. Bhatia et al., in their study, have shown reduced placental weight in severe toxemia of pregnancy and the lowest recorded was 280 g.[13],[14]
We also noted that the mean fetoplacental ratio was higher in the hypertensive group than in the control group, however, the data were not statistically significant.
In our current study, it revealed that subchorionic fibrin deposition/fibrinoid necrosis was a common occurrence among the placentae of hypertensive mothers. Out of fifty of the placentae from the hypertensive group, 50% showed evidence of subchorionic fibrin deposition whereas it occurred in only 10% of placentas from the control group. Navbir in 2012 inferred in their study that 90% of the PIH cases had evidence of subchorionic fibrin deposition.[15] Kambale et al., 2016, observed that 4.4% of placentae from the control group showed the presence of fibrinoid necrosis whereas it is present in 46.7% of placentae from the PIH group.[16] Porwal et al. in 2017 reported a presence of fibrinoid necrosis in 33% of the cases.[17]
Retroplacental hematoma is a hematoma occurring between the basal plate of the placenta and the uterine wall. It is apparent on the maternal aspect and bulges toward the fetal aspect. An old hematoma is adherent to the placenta, but a fresh one may get separated during the delivery process which is evident by a characteristic crater-like depression on the maternal surface. In our present study, 24% of placentas from the hypertensive mothers showed evidence of retroplacental hematoma, whereas 6% of placentas from the control group showed evidence of the same. Page et al. observed 0.8% and 6.2% retroplacental hematoma in the normal and PIH groups, respectively, whereas Kurdukar et al., 2007, noted a percentage of 12% and 12.2%.[18],[19]
Hypertension in pregnancy leads to increased maternal vasospasm, obliterative endarteritis, and decreased uteroplacental blood flow, all of which lead to increased incidence of infarction in the placenta. In our study, 46% of the placentas from the hypertensive group showed the presence of significant infarction (>5% surface area), whereas 10% of the placentas from the control group showed a similar feature. Dutta et al., 2017, also showed the presence of infarction in 78% of the cases.[20]
In the present study, 44% of the placentas in the hypertensive group showed evidence of calcification, but only 6% of the placentas from the control group revealed the same. Dutta et al. reported the incidence of calcification to be 50% in their study group.[20] Nahar et al., 2015, and Salmani et al., 2014, also reported an increased presence of calcification in placenta of hypertensive mothers.[10],[21]
In the present study, we found a statistically significant correlation between the presence of subchorionic fibrin and low birth weight delivery. Nigam et al. in 2014 conducted a case–control study performed at Medical College Allahabad to conclude that subchorionic fibrin was seen in significantly higher number of placentae from patients presenting with low birth weight delivery which corroborates the finding of our study.[22]
In our study, the incidence of neonatal deaths was 6% in the hypertensive group, whereas there was only 2% incidence of neonatal death in the control group. A study by Saadat et al. in 2007 reported an incidence of 5.6% fetal death among hypertensive mothers which was higher than found in this study.[23]
| Conclusion | | |
Hypertensive disorders complicating pregnancy are common and form one of the deadly triads along with hemorrhage and infection that results in large number of maternal deaths and therefore fetal deaths. From the present study, we concluded that hypertensive disorders of pregnancy cause significant histomorphological changes in placenta. Reduced placental weight, thickness, and diameter were noted on gross findings, whereas increased incidence of subchorionic fibrin, calcification, infarction, and retroplacental hematoma was detected microscopically. Furthermore, we also concluded that the changes in placenta are associated with the adverse fetal outcome in terms of low birth weight or low Apgar score in newborns to cases with PIH.
Financial support and sponsorship
Nil
Conflicts of interest
There are no conflicts of interest.
| References | | |
| 1. | Shan N, Zhang X, Xiao X, Zhang H, Chen Y, Luo X, et al. The Role of Laminin α4 in Human Umbilical Vein Endothelial Cells and Pathological Mechanism of Preeclampsia. Reprod Sci 2015;22:969-79.  |
| 2. | Chaiworapongsa T, Chaemsaithong P, Yeo L, Romero R. Pre-eclampsia part 1: Current understanding of its pathophysiology. Nat Rev Nephrol 2014;10:466-80. |
| 3. | Hypertension in pregnancy. Report of the American College of Obstetricians and Gynecologists' Task Force on Hypertension in Pregnancy. Obstet Gynecol 2013;122:1122-31. |
| 4. | Lambert G, Brichant JF, Hartstein G, Bonhomme V, Dewandre PY. Preeclampsia: An update. Acta Anaesthesiol Belg 2014;65:137-49. |
| 5. | Soma H, Yoshida K, Mukaida T, Tabuchi Y. Morphologic changes in the hypertensive placenta. Contrib Gynecol Obstet 1982;9:58-75. |
| 6. | Majumdar S, Dasgupta H, Bhattacharya K, Bhattacharya A. A study of placenta in normal and hypertensive pregnancies. J Anat Soc India 2005;54:1-9. |
| 7. | Teasdale F. Histomorphometry of the human placenta in pre-eclampsia associated with severe intrauterine growth retardation. Placenta 1987;8:119-28. |
| 8. | Cibils LA. The placenta and newborn infant in hypertensive conditions. Am J Obstet Gynecol 1974;118:256-70. |
| 9. | Londhe, P.S. and Mane. Placental Morphometry in Relation to Birth Weight of Full Term Newborn Babies. National Journal of Integrated Research in Medicine 2012; 3:67-72. |
| 10. | Salmani D, Purushothaman S, Somashekara SC, Gnanagurudasan E, Sumangaladevi K, Harikishan R, et al. Study of structural changes in placenta in pregnancy-induced hypertension. J Nat Sci Biol Med 2014;5:352-5. |
| 11. | Shahida S, Boota M, and Shahzad S. “Eclampsia.” Professional Medical Journal-Quarterly [The] 2006;13:27-31. |
| 12. | Bazaz G, Mirchandani JJ, Chitra S. Placenta in intrauterine growth retardation. J Obstet Gynaecol India 1979;29:805-10. |
| 13. | Nobis P, Das U. Placental morphology in hypertensive pregnancy. J Obstet Gynecol 1991;41:166-9. |
| 14. | Bhatia A, Sharma SD, Jalnawalla SF, Sagreiya K. A comparative study of placental pathology and fetal outcome. Indian J Pathol Microbiol 1981;24:277-83. |
| 15. | Navbir P. Placental morphology and its co-relation with fetal outcome in pregnancy-induced hypertension. Int J Basic Appl Med Sci 2012;2:120-5. |
| 16. | Kambale T, Iqbal B, Ramraje S, Swaimul K, Salveet S. Placental morphology and fetal implications in pregnancies complicated by pregnancy induced hypertension. Med J Dr. DY Patil Univ 2016;9:341-47. |
| 17. | Porwal V, Jain D, Gupta S, Khandelwal S, Kasliwal N .Spectrum of placental changes in pregnancy induced hypertension. Ann Pathol Lab Med 2017;4:A69 76. |
| 18. | Page EW. On the pathogenesis of pre-eclampsia and eclampsia. BJOG 1972;79:883-94. |
| 19. | Kurdukar MD, Deshpande NM, Shete SS, Zawar MP. Placenta in PIH. Indian J Pathol Microbiol 2007;50:493-7. [ PUBMED] |
| 20. | Dutta A, Sahu R. K., Chatterjee K, Kothari S, Rahaman S. K. R, Sen S. Placental damages from ultrasonic changes to histopathological findings in maturing placenta in pregnancy complicated with hypertension: An observational clinical study. Int J Reprod Contracept Obstet Gynecol 2017;6:1834-42. |
| 21. | Nahar L, Nahar K, Hossain MI, Yasmin H, Annur BM. Placental changes in pregnancy induced hypertension and its impacts on fetal outcome. Mymensingh Med J 2015;24:9-17. |
| 22. | Nigam J, Misra V, Singh P, Singh P, Chauhan S, Thakur B. Histopathological study of placentae in low birth weight babies in India. Ann Med Health Sci Res 2014;4:S79-83. |
| 23. | Saadat M, Marzoughian S, Gholamreza N, Mehrdad H. Maternal and neonatal outcomes in women with preeclampsia. Taiwan J Obstet Gynecol 2007;46:255-9. |
[Figure 1], [Figure 2], [Figure 3], [Figure 4]
[Table 1], [Table 2], [Table 3]
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